ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Expression of human amyloid precursor protein in rat cortical neurons inhibits calcium oscillations.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 57 citations in OpenAlex.
- Knockdown of Amyloid Precursor Protein Increases Ion Channel Expression and Alters CaInternational journal of molecular sciences · 2023Article
- Modulation of L-type calcium channels in Alzheimer's disease: A potential therapeutic target.Computational and structural biotechnology journal · 2023Review
- Tau isoform-specific enhancement of L-type calcium current and augmentation of afterhyperpolarization in rat hippocampal neurons.Scientific reports · 2022Article
- Human microRNA (miR-20b-5p) modulates Alzheimer's disease pathways and neuronal function, and a specific polymorphism close to the MIR20B gene influences Alzheimer's biomarkers.Molecular psychiatry · 2022Article
- APPsα rescues impaired CaProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Implications of Oligomeric Amyloid-Beta (oAβThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Alterations of the Endoplasmic Reticulum (ER) Calcium Signaling Molecular Components in Alzheimer's Disease.Cells · 2020Review
- Amyloid, APP, and Electrical Activity of the Brain.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2020Review
- How TRPC Channels Modulate Hippocampal Function.International journal of molecular sciences · 2020Review
- Presenilin-Deficient Neurons and Astrocytes Display Normal Mitochondrial Phenotypes.Frontiers in neuroscience · 2020Article
- APP as a Protective Factor in Acute Neuronal Insults.Frontiers in molecular neuroscience · 2017Review
- Accumulation of human full-length tau induces degradation of nicotinic acetylcholine receptor α4 via activating calpain-2.Scientific reports · 2016Article
- Templated misfolding of Tau by prion-like seeding along neuronal connections impairs neuronal network function and associated behavioral outcomes in Tau transgenic mice.Acta neuropathologica · 2015Article
- Unfolded Protein Response and PERK Kinase as a New Therapeutic Target in the Pathogenesis of Alzheimer's Disease.Current medicinal chemistry · 2015Review
- New in vitro phenotypic assay for epilepsy: fluorescent measurement of synchronized neuronal calcium oscillations.PloS one · 2014Article
- Amyloid precursor protein controls cholesterol turnover needed for neuronal activity.EMBO molecular medicine · 2013Article
- Amyloid Beta-Protein and Neural Network Dysfunction.Journal of neurodegenerative diseases · 2013Review
- Nebula/DSCR1 upregulation delays neurodegeneration and protects against APP-induced axonal transport defects by restoring calcineurin and GSK-3β signaling.PLoS genetics · 2013Article
- Functional consequences of the lack of amyloid precursor protein in the mouse dentate gyrus in vivo.Experimental brain research · 2012Article
- Physiological functions of APP family proteins.Cold Spring Harbor perspectives in medicine · 2012Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synchronous calcium oscillations are observed in primary cultures of rat cortical neurons when mature networks are formed. This spontaneous neuronal activity needs an accurate control of calcium homeostasis. Alteration of intraneuronal calcium concentration is described in many neurodegenerative disorders, including Alzheimer disease (AD). Although processing of amyloid precursor protein (APP) that generates Abeta peptide has critical implications for AD pathogenesis, the neuronal function of APP remains unclear. Here, we report that expression of human APP (hAPP) in rat cortical neurons increases L-type calcium currents, which stimulate SK channels, calcium-dependent K(+) channels responsible for medium afterhyperpolarization (mAHP). In a neuronal network, increased mAHP in some neurons expressing hAPP leads to inhibition of calcium oscillations in all the cells of the network. This inhibition is independent of production and secretion of Abeta and other APP metabolites. In a neuronal network, reduction of endogenous APP expression using shRNA increases the frequency and reduces the amplitude of calcium oscillations. Altogether, these data support a key role for APP in the control of neuronal excitability.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.